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Finally, Gly91 was removed from VEGF-B segment because of low intrinsic propensity to form -sheet structure, and Gln87 was removed from VEGF-A segment as this residue does not participate in the interaction with VEGFR2 (Fig

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Various techniques assessed marker expression, transcriptomic profiles, and in vitro cell experiments with BV2 cells

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We focus on documented outcomes in hypermobile and classical EDS (which feature pronounced joint laxity), and discuss one example in the vascular subtype